Down-regulation of integrin αMβ2 ligand-binding function by the urokinase-type plasminogen activator receptor

2006 ◽  
Vol 348 (3) ◽  
pp. 1184-1193 ◽  
Author(s):  
Man-Li Tang ◽  
Le-Sheng Kong ◽  
S.K. Alex Law ◽  
Suet-Mien Tan
Keyword(s):  
Ligand Binding ◽  
Plasminogen Activator ◽  
Down Regulation ◽  
Binding Function ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Plasminogen Activator Receptor

scholarly journals Down-regulation of Integrin αvβ3Expression and Integrin-mediated Signaling in Glioma Cells by Adenovirus-mediated Transfer of Antisense Urokinase-type Plasminogen Activator Receptor (uPAR) and Sensep16Genes

2001 ◽  
Vol 276 (50) ◽  
pp. 47171-47177 ◽  
Author(s):  
Yoshiaki Adachi ◽  
Sajani S. Lakka ◽  
Nirmala Chandrasekar ◽  
Niranjan Yanamandra ◽  
Christopher S. Gondi ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Intracellular Signaling ◽  
Cell Biology ◽  
Glioma Cell ◽  
Biological Effects ◽  
Glioma Cells ◽  
Down Regulation ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Plasminogen Activator Receptor

Interaction between the extracellular matrix and integrin receptors on cell surfaces leads not only to cell adhesion but also to intracellular signaling events that affect cell migration, proliferation, and survival. The vitronectin receptor αvβ3integrin is of key importance in glioma cell biology. The expression of urokinase-type plasminogen activator receptor (uPAR) was recently shown to co-regulate with the expression of αvβ3integrin. Moreover, restoration of the p16 protein in glioma cells inhibits the αvβ3integrin-mediated spreading of those cells on vitronectin. Thus we hypothesized that adenovirus-mediated down-regulation of uPAR and overexpression of p16 might down-regulate the expression of αvβ3integrin and the integrin-mediated signaling in glioma cells, thereby defeating the malignant phenotype. In this study, we used replication-deficient adenovirus vectors that contain either a uPAR antisense expression cassette (Ad-uPAR) or wild-type p16 cDNA (Ad-p16) and a bicistronic adenovirus construct in which both the uPAR antisense and p16 sense expression cassettes (Ad-uPAR/p16) are inserted in the E1-deleted region of the vector. Infecting the malignant glioma cell line SNB19 with Ad-uPAR, Ad-p16, or Ad-uPAR/p16 in the presence of vitronectin resulted in decreased αvβ3integrin expression and integrin-mediated biological effects, including adhesion, migration, proliferation, and survival Our results support the therapeutic potential of simultaneously targeting uPAR and p16 in the treatment of gliomas.

scholarly journals Inhibiting the urokinase-type plasminogen activator receptor system recovers STZ-induced diabetic nephropathy

2018 ◽  
Vol 23 (2) ◽  
pp. 1034-1049 ◽  
Author(s):  
Massimo Dal Monte ◽  
Maurizio Cammalleri ◽  
Valeria Pecci ◽  
Monica Carmosino ◽  
Giuseppe Procino ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Plasminogen Activator ◽  
Receptor System ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Plasminogen Activator Receptor
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